Systemic lupus erythematosus (SLE) is a multi system autoimmune disease manifested by autoantibody production, arthritis, skin rash, nephritis, cytopenias, and vasculitis. The etiology of this disease is unknown, but recent studies suggest a role for nitric oxide (NO). NO is a soluble intercellular messenger involved in vasodilation, neurotransmission, anti-tumor and anti-microbial activity, and inflammation. In murine autoimmune modes, elevated NO production parallels the onset of disease. If NO production is blocked, clinical and pathologic evidence of disease diminishes significantly, indicating a critical role for NO in autoimmunity in these models. Patients with SLE have enhanced systemic NO production in peripheral blood mononuclear cells (PBMCs) parallel disease activity in patients with SLE. This study will also investigate potential mediators of NO production in PBMCs of control and SLE subjects. Finally, the study will determine the effects of NO on apoptosis of control and SLE PBMCs. A simple, inexpensive marker for impending disease flares could emerge from the results of this study. In addition, if this investigation provides further understanding regarding the cause or effect of elevated NO production in SLE, more specific and thus more effective and less toxic therapies could emerge.